sanatate kinetica.doc

7/29/2019 sanatate kinetica.doc

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Muscle Imbalance: The Goodheart and Janda

Models

By Scott Cuthbert, BA, DC, BCAO

Evidence suggests measurable muscular inhibition (weakness) is associated with injury,inflammation and pain, as reviewed in my recent four-part series in this publication.1-4 This

evidence is part of the rationale for the chiropractic physician's use of the manual muscle test

(MMT) for the assessment of muscular inhibition in our patients.

Muscular imbalance is the combination of weakness and hypertonicity (tightness); however,

there are differing approaches as to the diagnosis and treatment of these muscular imbalance

phenomena that are a fundamental component for patients with manipulable disorders.

The voluntary skeletal muscle system is the largest single organ in the body. It measures in at

over 40 percent of body weight and is maintained in a sophisticated state of balance and

coordination throughout a wide range of postures and activities. The muscles are at once the

source and the recipient of the greatest neural activity in the body. This includes sensory and

motor activity, segmental and cerebral pathways, plus autonomic activity in relationship to the

metabolic, visceral, and circulatory demands required during human movement.

The focus of treatment for muscular imbalance is where the Goodheart and Janda models

divide. Goodheart and Janda agreed that the muscles are in fact "the most exposed part of the

nervous system." Muscle imbalance therefore brings us back to the nervous system, which is

at the core of all human activity - this is where D.D. Palmer started from in the first place.

George J. Goodheart Jr., DC (1918-2008) and Vladimir Janda, MD (1923-2002) influenced

generations of practitioners spanning many disciplines. One difference between Goodheart's

approach (a chiropractor) and Janda's (a physical therapist) is that muscle inhibitions are

identified and treated first with chiropractic manipulative therapy (CMT). In agreement with

the literature cited in previous articles, muscle inhibition is seen as an etiological factor and/orcommon co-factor in neck, low back, and extremity pain and dysfunction.1-4, 5

Sherrington's law of reciprocal innervation states that muscle inhibition usually generates

hypertonicity/tightness in antagonist muscles, and that the relationship between weak and

tight muscles is reciprocal, with inhibition producing the same influence on their antagonist

muscles as tightness. Sherrington advises that "Knowledge of reflex inhibition equally with

that of reflex excitation is essential for the study of nervous co-ordination."6 This means that

abnormal muscle inhibition is as neurologically important as over-facilitation in patients with

pain and dysfunction.

In fact, Lund and others have confirmed Sherrington's early insights, showing that inhibition is

frequently found in muscles resulting from injury, inflammation or pain and that the inhibition

or weakness leads to reciprocal facilitation of its antagonist(s) and aberrant behavior of itssynergist(s).1-4, 7 It is also true that hypertonicity in a muscle leads to reciprocal inhibition of its

antagonist(s) and aberrant behavior of its synergist(s).8 This is the reciprocity of Sherrington's

Law, with due respect paid to both the Goodheart and Janda models of diagnosis and

treatment for muscular imbalance.


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Hypertonic muscle secondary to inhibited muscle and

inhibited muscle responsive to chiropractic manipulative therapy (Goodheart model). Goodheart's model is

the one used by members of the chiropractic profession who employ the MMT for diagnosis of

neuromusculoskeletal dysfunction.9-11 Inhibited muscles found in the chiropractic setting are

capable of spontaneous strengthening when the inhibitory reflex is identified and remedied

(most commonly through joint or soft-tissue manipulation).

In Janda's model, Sherrington's Law of reciprocal innervation operates primarily in one

direction: Muscle hypertonicity/tightness/spasm generates inhibition in its antagonists, and so

spasm is treated first. For this reason, muscle spasm and tightness are considered the

etiological factors of articular dysfunction. In Janda's approach, hypertonic muscles are treated

with physiotherapeutic means such as massage, stretching, proprioceptive neuromuscular

facilitation, electrotherapy and other methods that do not usually include CMT.12-13 In Janda's

classic text on MMT, there is little mention of spinal or other joint manipulation options for themuscle inhibitions found, and no correlations are observed between manipulative corrections

(or cranial, meridian, nutritional, or psychological treatments) for specific muscle inhibitions.8

In Janda's model, the inhibited (weak) muscles are treated with exercise, rocker boards,

wobble boards, balance shoes, and mini trampolines, among other strategies. The principles of

this physical therapy approach to muscular imbalances were based on the work of Bobath and

Bobath, who developed physiotherapy programs for children with cerebral palsy.14

It is of major concern that patient compliance and participation is poor for exercise programs.

Most rehabilitation, stretching, and exercise programs report a reduction in patient

participation (even when the individuals felt that the effort was producing benefits).15

Correcting muscle inhibitions with remedial exercise is quite time-consuming, and patients are

remarkable in how incorrectly they perform their exercises. Although chiropractors employexercise and rehabilitation programs in their treatment of patients, they focus their unique

training and skills to provide CMT for correction of neurological inhibitions. Furthermore,

articular dysfunctions that produce muscle inhibition in patients will not be effectively

addressed with exercise, stretching, and other non-manipulative modalities.

Janda asserted throughout his remarkable career that postural muscles tend to be short and

tight and usually hypertonic. However, the current literature does not always agree with

Janda's classification of which muscles are "postural" or "phasic."16 Janda's conception that
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postural muscles tend to be tight and phasic muscles tend to be weak is too restrictive, as

shown by many studies that suggest postural muscles are so often inhibited in physical

disturbances, especially low back and neck pain.1-4, 17 Muscle fiber types (tonic and phasic, and

slow-twitch and fast-twitch) are not fixed and evidence shows the potential for adaptability of

muscles based on use and need, so thatmuscle fibers can be transformed from slow

twitch to fast twitch and vice versa.18

Naming the muscle category and then treating the category is equivalent to giving all patients

a general adjustment, or the same all-purpose multivitamin pill.

It is the clinical experience of manual muscle testers that muscle imbalances relate primarily

to the individual patient's adaptations to specific injuries and stresses, rather than to any

properties of these muscles to be either hypotonic or hypertonic as a rule. If a muscle

becomes hypotonic or hypertonic, this occurs as a result of a lifetime of adaptive neurological

events in a patient's history, and not because a particular muscle is "postural" or "phasic." The

fact that postural muscles frequently show inhibition on MMT assessment is more in line with

the common impression that painmakes muscles difficult to use and less powerful.19

There is considerable variability in the changes of muscle activity between individuals with

neck pain, as demonstrated by the large standard deviation of EMG data.2, 20 Edinger as well asStrong showed that individuals with leg-length inequality who placed their feet in a normal

position a few inches apart showed substantial individual variations in the standing EMG.21-22

In the Goodheart model, if muscle inhibition is caused by a manipulable articular or soft-tissue

disorder, then the inhibited muscle's response to the proper CMT will be immediate and the

tight antagonist muscles will relax. This brings about postural balance on visual inspection and

corrects the positive MMT findings, both of which are evidence of the muscle imbalance

phenomena.

A risk with Janda's model of muscle dysfunction is that practitioners may expect to find set

changes to occur and fail to adequately assess the patient's genuine state. This can result in

poor treatment outcomes. Every muscle that is part of an articular and postural dysfunction

(or part of a kinematic chain of muscular dysfunction) must be specifically assessed for

strength, coordination, ease of use, length and tone, no matter what model you follow

clinically.

Although the distinctions between hypotonic and hypertonic muscles (including Janda's upper-

and lower-crossed syndromes) can usefully assist the clinician, they are not cast in stone.

Diagnosis of muscular imbalances underlying articular dysfunctions must be refined to reveal

the subtleties of the muscle system's reactions to injury, pain, altered use and pathology in

the particular patient under study.

Goodheart points out that muscular adaptation can involve a wide variety of influences

(structural, chemical and mental).9 The chiropractor therefore must keep in mind that what is

presented and observed in a patient with muscle imbalances may represent only the acuteproblems that brought the patient in for care, which have evolved out of chronic adaptive

patterns. Discovering the core of the problem and diagnosing the treatable obstacles to normal

function involves patience, adaptability and skill; and if you are using chiropractic hands-on

treatment methods, the correct model of muscle imbalance helps.

Experienced clinicians agree that unpredictability and individuality are the rule where muscular

compensations are concerned, especially when recent adaptations are added onto chronic

adaptation patterns in the typical patient. In the case of the muscle imbalance phenomenon,

this should lead clinicians to evaluate individual muscles in individual humans with the MMT. In
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Neuromuscular Function

The conscious decision for movement is made from the brain sending nerve impulses to themuscles for the production of muscle force and joint motion (motor pathways).

Sensory receptors in the muscles, skin, ligaments and joints reflexively modify muscle force andrelays nerve impulses back to the brain communicating the position of the joint at any moment intime (sensory pathways).

Motor and sensory pathways interact to provide the proper muscle length, tension and tone formovement and posture (neuromuscular function).

Joint Dysfunction

Poor neuromuscular function is either the cause or the effect of unnatural changes in joint mobilityand stability (joint dysfunction).

Unnatural Joint Mobility

Changes in the freedom of joint motioncaused by inflexible muscles, tissue

length adaptation, weakness

Unnatural Joint Stability

Changes in finely tuned motion controlcaused by mobility issues, fatigue,

reflexive signaling

Effects

Increased muscle stiffness and activationlevels, movement asymmetry,

compensation patterns, joint alignment

changes

Effects

Decreased mobility, joint alignment,balance, timing muscular coordination,

efficiency and muscular weakness

1. Movement-Based Problems

Joint dysfunction causes predictable compensations in the movement pattern of the kinetic chain.

Movement compensations during physical activity increases problematic stress of muscles,tendons, ligaments and bones at the neighboring joint above or below the dysfunctional joint.

Movement-based problems of the kinetic chain decreases athletic performance, increases the riskof injury and prevents recovery from injury.


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The Kinetic Chain

The body is a series of moving segments linked by joints. (figure 1)

Joint motions are produced by the muscles, influenced by gravity and controlled by the nervous

system.The sequencing of multiple joint motions and muscle activations to produce purposeful movementor posture is known as the kinetic chain.


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Joint Mobility and Stability

The motion of every link within the kinetic chain requires an optimal combination of mobility andstability.

Each kinetic chain link has a greater functional need for either more mobility or more stability. (figure2)

The functional preference for mobility or stability alternates between joints from head to toe.


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Movement Patterns

Multiple mobile and stable joints working together in a coordinated manner produce a movementpattern.

Functional movement patterns of the kinetic chain produce efficient and effective movementsequences and posture.

The structural and functional interconnections of the kinetic chain produce predictable movementpatterns.

Movement Efficiency

Movement compensations, unresolved injuries, de-conditioning, poor lifestyle, stress, posturalhabits and pain are all contributing factors that lead to dysfunctional and inefficient movementpatterns.

The primary goal for movement training is to enhance the neuromuscular control of mobile andstable segments to produce efficient movement patterns.

Movement efficiency is used to improve:

Neuromuscular Control

Neuromuscular control is the interaction between motor and sensory pathways functioning toprovide the proper muscle length, tension, tone for efficient movement and posture of the kineticchain.

Compensatory movement patterns are a cause or an effect of muscular adaptations in stiffness(combination of length and tension) and tone which hinders the muscle's capacity to produce forceand relay quality sensory information to the brain.

Improvements in neuromuscular control without the support of compensatory muscle stiffness willinfluence joint motion, alignment, balance, timing, sub-maximal muscle quickness, coordination andactivation.

Regional Interdependence

Your body is an interconnected system. It consists of myofacial (muscles and connective tissues),articular (joints), and neural (brain and nerves) components. These components have to workclosely together and require the sequential coordination of each joint to be properly aligned, stableand mobile to create a movement pattern. The motion produced at any joint in the kinetic chaindirectly affects the joints above and below it, so, dysfunction in any one component influencing aparticular joint may have a direct and detrimental effect on the function of a neighboring joint.

The Ankles

Limited ability of the foot to bend up and down at the ankle will influence rotation at the lower legand cause the foot to roll too far in or out. Balance, shock absorption and explosive athletic powerare compromised and increases stress to the compensating muscles of the knee and hop joints.


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Flat Feet and the Kinetic Chain

In order to understand the cause, effects, and ultimately the successful treatment

of flat feet it is necessary to not just examine the problem as isolated to the foot

but to also take into consideration the entire kinetic chain for which the foot is the

foundation.

Holistic: Characterized by comprehension of the parts of somethingas intimately interconnected and explicable only by reference tothe whole.

Most peoples arches form as a normal part of development in childhood. For

some individuals an arch never develops. Some studies have found a correlation

between the frequency of shoe wear and flat feet in children but further research

still needs to be conducted to answer the question of why wearing shoes hinders

the development of an arch. Do the shoes act directly on the muscles and

ligaments of the foot to weaken those structures or does footwear alter the

joint positioning and muscle activity higher up in the knee or hip?

The onset of flat feet is not just a

childhood problem. Adults can also acquire flat feet as part of the aging process.

Women and people over 40 are more likely to develop a problem with the known

risk factors being obesity, hypertension, and diabetes. Most cases of acquired

adult flat foot are linked to a dysfunction of the posterior tibialisa muscle

that runs along the inside of the leg and plays a major role in supporting

the arch. Why individuals develop posterior tibialis dysfunction and flat feet later

in life is also a matter of debate. Some studies have indicated that people with

posterior tibialis insufficiency often have a pre-existing flat foot. In some

instances this deformity may be so mild to have gone unnoticed but over time

this likely subjects the muscle to undue wear and tear, eventually leading to

degenerative changes.
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If a child or adult appears flat footed when their feet are in contact with the

ground but has a visible arch when not standing or when they raise up on their

toes this is called a flexible flat foot and is by far the most common type of flat

foot deformity. Because these individuals still have the capacity to form an arch

given the right circumstances its my contention that they still have the potential

to restore a normal arch if the right bio-mechanical problems are addressed.

While current research has shed light on some of the factors involved, it is

unlikely that we will ever identify just one single cause of flat feet due to

the number of variables involved. The foot and ankle alone have 26 bones, 33

joints, and over 100 muscles, tendons, and ligaments. In addition to this, the

ground reaction force generated when the foot make contacts with the ground

affects not just the foot and ankle but every joint of the lower limb. So instead of

focusing on a single structure the best approach would be to look at the body as

a whole and target any joint or muscle that can impact or be impacted by the

arch of the foot.

To start, lets examine what happens to the body in an individual with flat feet.

When the arch collapses the foot and

ankle complex goes into a hyper-pronated position. Pronation is actually

a combination of three different movements but it can easily be visualized as the

ankle rolling inward. Hyper- or over-pronation is an excessive collapse of the

joints that comprise the rear foot and ankle. This excessive movement sets off acascade of events that travel up the leg. The ankle rolling in produces torque

on the lower leg causing the tibia to also turn inward . Continuing up the leg,

the tibia articulates with the femur at the knee joint. Internal rotation of the tibia

will then cause both internal rotation and adduction (movement toward the

inside) of the femur at the hip joint. Even farther up, the hip is comprised of
http://www.somastruct.com/what-is-pronation/http://www.somastruct.com/wp-content/uploads/2012/06/pronationexplained3.jpghttp://www.somastruct.com/what-is-pronation/


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the head of the femur sitting in the acetabulum or socket of the pelvis. The

movement of the hip into internal rotation and adduction will then go on to

cause an anterior tilting of the pelvis (visualize the front of the pelvis

dropping down).

What I just described would be called

the kinetic chain, meaning that a change in one area will produce a movement

in all areas directly or indirectly connected to itlike a ripple effect. Some people

will argue that this process will continue up into the lower back and even higher

however studies are unclear whether the effects of pronation actually translate

past the pelvis. Even if the forces could travel that far their contributions would be

minimal because, like a ripple, the effects becomes weaker the farther out you go

so we will limit our investigation to the leg and pelvis. Now, I listed the jointmovements in order from the ground up, but the kinetic chain runs in both

directions. We could also go in reverse and say that each one of those

movements lower down in the leg is caused by a change in position of the joint

above it, starting at the pelvis. Because it is unclear to what degree each joint

contributes to the arch collapsing or in which order these aberrant motions

occurs it is best to take a wide view and direct our attention to any joint that may

be a contributing factor.

Having identified the joint movements associated with flat feet, itstime to examine the muscles and tendons that can produce orrestrict movement at those joints.

Your body is a well balanced feat of engineering. Almost every muscle will have

either a single muscle or a muscle group that produces an opposing movement

to its function. Often time dysfunctions in the musculoskeletal system are

described as imbalances. These are described either in terms of a muscle
http://www.somastruct.com/wp-content/uploads/2012/06/skeletoneffects.jpg


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or group overpowering the weak countering muscles, or certain muscles

being inflexible and consequently limited motion in the opposite direction.

If we look at each component along the kinetic chain there will be one set of

muscles that would resist or counteract that movment and these are the muscles

that need to be strengthened. Taking anteior pelvic tilting as an example we will

find weakness in the muscles that perform the opposing motion, posterior pelvic

tilting. As well as strengthening the muscles to allow improved posterior pelvic

tilting we would also then need to stretch the muscles that, if inflexible, would

oppose posterior tilting. This concept of identifying weak and tight muscles

can be applied to each joint motion that Ive listed related to flat feet:

Anterior Pelvic Tilt:

Weak hamstrings

Weak abdominals Weak glutes

Tighterector spinae

Tighthip flexors (mainly the iliopsoas and rectus femoris)

Internal Rotation of the Hip:

Weak gluteus maximus

Weak gluteus medius

Weak biceps femoris (lateral hamstring muscle)

Weak external rotator group (6 small muscles of the pelvis)

Tightgluteus minimus

Tightsemimembranosus and semitendinosus (medial hamstring muscles)

Tightadductor group

Tightpectineus

Adduction of the Hip:

Weak glutes (maximus, medius, and minimus)

Weak Tensor Fascia Lata (TFL)

Tightadductor group

TightpectineusInternal Rotation of the Tibia:

Mostly a passive movement related the pull of soft tissue on osseous

structures acting on the tibia and therefore controlling the movements of the

joints around the tibia will reduce the forces that produce this internal rotation

Weak biceps femoris


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Pronation of the Ankle and Foot:

Weak intrinsic foot muscles (abductor hallucis, flexor digitorum brevis etc.)

Weak posterior tibialis

Weak anterior tibialis

Weak extrinsic foot muscles (flexor hallucis longus, flexor digitorum

longus)

Tightperoneals (ankle evertors)

Tightgastrocsoleus (calf muscles) and Achilles tendon

Now you may notice some inconsistencies particularly in regards to the muscles

of the hip and hamstrings appear in both the weak and tight classifications. This

is because muscles may perform different functions depending on the positioning

of the joints. It is also important to note that while the joint movement patterns

listed above will likely hold true for most flat footed people, every individual will

present with varying degrees of weakness and inflexibility so it is best to

investigate muscle imbalances on a case by case basis. While muscle

imbalances are a major part of structural issues in the body, only treating these

issues will have limited benefit if other confounding variables, such as habitual

movement patterns or obesity, are not addressed as well.

Below is a table that provides a summary of the joint movements associated with

flat feet and the associated muscle imbalances to help serve as a framework for

generating a comprehensive treatment approach:

Strengthen Stretch

Pronation Supinators: Intrinsic and

Extrinsic Foot Muscles,

Tibialis Posterior and

Anterior

Pronators: Gastrocsoleus,

Peroneals, Achilles Tendon

Tibial Internal Rotation Hamstrings, Tibialis

Posterior

Pronators: Gastrocsoleus,

Peroneals, Achilles Tendon

Hip Adduction Hip Abductors Hip Adductors, Pectineus

Hip Internal Rotation Hip External Rotators,

Glutes

Hip Adductors, Hamstrings

Anterior Pelvic Tilt Abdominals, Hamstrings Hip Flexors, Erector Spinae


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